Wk 2 Antivirals Flashcards

(71 cards)

1
Q

When do antivirals work?

A

it must get inside the host cells when the virus is still replicating

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2
Q

Often times, the virus has finished…

A

replicating when signs and symptoms develop

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3
Q

Antivirals can also kill…

A

healthy cells

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4
Q

A virus is a __ microbe

A

parasitic

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5
Q

Viruses do not have a __ __ of their own

A

cell wall

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6
Q

How does a virus live?

A

Inserts it’s own DNA or RNA into our cells

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7
Q

List some viruses we are able to treat

A

HSV, HZV, flu, RSV, HIV, CMV, hepatitis

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8
Q

What is acyclovir used to treat?

A

HSV

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9
Q

What are the routes for acyclovir?

A
oral
tablets
liquid
topical
IV
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10
Q

3 MOA of acycolvir

A

Interferes with nucleic acid synthesis
Prevents virus from binding
Stimulates immune response

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11
Q

Acyclovir side effects

A

Gi distress, renal impairment, seizures, ITP

Tissue necrosis in IV form

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12
Q

The shingles vaccine is a __ vaccine

A

live

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13
Q

What is Shringrix?

A

Herpes zoster vaccine for those over 50

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14
Q

What does oseltamivir do?

A

mostly active against flu A but also some flu B

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15
Q

What is the MOA of oseltamivir?

A

Inhibits neuroamidases

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16
Q

What route is oseltamivir?

A

only PO

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17
Q

What are the side effects of oseltamivir?

A

N/V
seizures
renal impairment

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18
Q

What is ganciclovir?

A

antiviral that treats cytomegalovirus (CMV)

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19
Q

Who is ganciclovir for?

A

Immunosuppressed people like HIV or transplant patients

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20
Q

What is the MOA of ganciclovir?

A

Inhibits DNA polyamerases, stops replication

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21
Q

What routes are ganciclovir?

A

IV and PO

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22
Q

If you crush ganciclovir and get it on your skin, what should you do?

A

wash hands with soap and water

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23
Q

What are the black box warnings for ganciclovir?

A

Hematologic toxicity
Fertility impairment
Fetal toxicity
Carcinogenesis

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24
Q

Who has the highest prevalence of HIV?

A

Black men

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25
What does HIV target?
CD4 on t cells
26
a mutation of __ actually blocks some strains of HIV from entering the cell
CCR5
27
First HIV __ to the cell membraine
fuses
28
Once inside HIV
replicates inside the cell and then moves into the nucelus
29
Final stage of replication, the virus creates
HIV protease
30
What re the 7 stages of HIV replication
``` Binding Fusion Reverse transcription Integration Replication Assembly Budding ```
31
A TB skin test for a patient with HIV will be...
False negative
32
What does HIV use to replicate after it has been integrated into the nucleus?
protease
33
What are the hallmarks of HIV infection?
Decrease in CD4 t helper cells | Proliferation of HIV particles
34
What is a normal cd4 t cell count?
Between 500-1500
35
Early stage of HIV
No antibodies Infectious Seroconversion - flu like symptoms
36
Clinical latency/chronic HIV
Last 3-12 yrs Asymptomatic or mild symptoms Stable virus levels
37
Rapid virus production
body defenses are less effective and person enters symptomatic stage of HIV, has AIDS
38
AIDS is CD4 count below
200
39
Thrush is often seen in the __ phase of HIV
acute
40
White lesions on lateral margins of the tongue occur in
all stages of HIV infection, oral hairy leukoplakia
41
periodontal disease is common in
all stages of HIV
42
What are fungal aids defining illnesses
Pulmonary/esophageal candidiasis | Pneumocystitis carinii jiroveci pneumonia
43
What are viral aids defining illnesses
CMV | HSV chronic ulcer over a month, pulmonary or esaphageal
44
What are protozoal aids defining illnesses
toxoplasmosis isoporiasis cryptosporidiosis
45
What are bacterial aids defining illnesses
mycobacterium recurrent pneumonia salmonella septicemia
46
What are cancerous aids defining illnesses?
Kaposi's sarcoma Cervical cancer Lymphomas
47
3 other aids defining illnesses
Wasting syndrome Encephalopathy AIDS demential complex
48
Why has HIV associated dementia decreased?
antiretroviral therapy
49
4 reasons someone who is exposed doesn't develop HIV
Duration/frequency of contact Concentration of virus Host immune status Genetic protective factors - defective ccrd
50
3 methods of transmission
unprotexted sex parenteral mother-child
51
3 things that further increase risk of HIV
oral sex anal sex lack of circumcision
52
How long are babies treated after being born for HIV?
6 weeks
53
Combination of 3 or 4 drugs to treat HIV is called...
HAART - highly active anti retroviral therapy
54
3 reasons to use HAART instead of mono therapy
delay or reserve loss of immune function prplongs life decreases aids related complications
55
What are the drawbacks of HAART?
Expensive long term side effects drug interactions life long
56
CCR5 antagonist
Maraviroc
57
Fusion inhibitor
Enfurvirtide
58
Protease Inhibitor
Lopinavir/Ritonavir
59
Integrase Inhibitor
Raltegravir
60
Reverse transcript inhibitors
Zidovudine | Efavirenz
61
Zidovudine NRTI side effects
Severe anemia and neutropenia | Lactic acidosis in female or obese patients
62
Efavirenz NNRTI side effects
Rash, CNS symptoms | Inhibits p450 system drug interactions
63
Reltegravir side effects
Well tolerated | Metabolized but UGT caution with other UGT inhibitors
64
Lopinavir/Ritonavir side effects
Hyperglycemia, lipodystrphy, hyperlipidemia, bones loss
65
Enfuvirtide side effects
sq bidInjection site reactions Pneumonia Hypersensitivity
66
Maraviroc side effects
Only works with certain strains of HIV, black box liver, drug interaction CYP 3A4. Teach about signs of reaction
67
What is prep?
Trivada for those at highest risk of new infection
68
How often are patients on prep followed up with HCP?
every 90 days
69
What is pep?
Post exposure prophylaxis
70
When should pep be administered?
2-3 hours after exposure, effectiveness reduced after 72 hours
71
When is person on pep tested?
6 and then 12 weeks after exposure